From PNAS:
Duplicate genes are essential and ongoing sources of genetic material that evolution can act on, yet new duplicates are under constant risk of being inactivated by mutations and subsequently lost. We show that a common heritable epigenetic modifier, DNA methylation, plays an important role in duplicate gene evolution. DNA methylation clearly distinguishes young and old duplicates, and the differences in DNA methylation of duplicate genes are associated with functional differences in expression. Remarkably, for a majority of duplicate gene pairs, a specific duplicate partner is consistently hypo- or hypermethylated across highly divergent tissues. Our results indicate that epigenetic modifications are intimately involved in the regulation and maintenance of duplicate genes.
From the Abstract ⌠Remarkably, many duplicate gene pairs exhibit consistent division of DNA methylation across multiple, divergent tissues: For the majority (73%) of duplicate gene pairs, one partner is always hypermethylated compared with the other. âŚ
Should we tell that guy who is standing athwart epigenetics and yelling âStop!â?
See also: Richard Dawkins responds to âDie, Selfish Gene, Dieâ: Mere adversarial journalism
Epigenetics: Inheritance of acquired traits gradually gaining acceptance
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Apart from that buzzword “epigenetics”, what do you think this research shows? How do you it related to your recent fascinatation with the “limits” of DNA?
wd400,
How about this for starters: What even remotely realistic proposal do Darwinists have for how in the world did a system which regulates the entire development of the body-through turning on and off switches which decide what genes will do, and is a fundamentally essential structure of the living unit, develop through a step by step series of copying mistakes which accidentally confer small advantages?
Nice try phoodoo, but instead of running the distraction why don’t you answer the question?
I think that this is highly intriguing research. If a duplicate gene happens, it is disabled. The darwinian presumption seems to be that this will give it the advantage of floating in the aether of random mutation with the chance of coming up with something wonderful. This is balderdash. In “Edge of Evolution” Behe clearly shows that once two mutations have bombarded the DNA, it is toast!
The disabling of duplicate genes, in my opinion, all but eliminates them as a candidate for co-option. This report is bad news for the honest darwinist.
WD400
I’ll give your question a go…..
Firstly, what we see here is a real regulation mechanism, I have to ask how does it “know” what is to be regulated?
http://www.investorwords.com/7.....ystem.html
This is a real example of design in biology it’s not even an analogy……
Andre:
Very good point. đ
The regulation by differential methylation makes no sense under the premise that the duplicated gene is the product of random events, and that its further “evolution” is still the product of random events.
Even is random events are implied (which, at this point, is clearly not certain), I would say that there is a name for random events regulated and controlled by definite algorithms: it’s “bottom up engineering”. IOWs, design.
wd400 you complain:
Now this, especially the ‘running the distraction’ part, is a extremely ironic statement for you to make. For I have seen you, instead of ever being honest towards the evidence, constantly ‘running the distraction’ here on UD. In fact, as I’m sure you well remember, Mr. Arrington recently ran a post featuring your lack of honesty towards the evidence when you were called on a literature bluff (i.e. ‘running the distraction’):
Now wd400, the following is a very, very, simple point that doesn’t take a advanced degree, or advanced mathematics, to understand. In science, empirical evidence has the last word as to whether a theory is true or not. Darwinism has no empirical evidence that it can generate complex novelty of even a trivial kind so as to prove it is true. In fact, the following study surveys four decades of experimental work, and solidly backs up the conclusion that there has never been an observed violation of what is termed ‘genetic entropy’ by purely material processes:
Moreover, if you go through the studies in the preceding paper, you will find that the small fraction of ‘gain of function’ mutations that don’t ‘degrade the genome to a greater or lesser extent’ are found in the experiments where ‘compensatory mutations’ are allowed to repair a organism after information was subtracted from the organism. Which is all great if you are trying to prove that organisms are ingenuously designed to repair themselves after damage, but is bad news if you are trying to prove that Darwinian processes can generate information over and above what is already present in life! There is even a null hypothesis in place stating that purely material processes can NEVER generate functional information (D. Abel)!
Many more notes along the same line, demonstrating the abject failure of Darwinian processes to ever ‘deliver the goods’ empirically, are gone over here:
Now wd400, I know you are quite a clever fellow by the way you are continually, to use your words, ‘running the distraction’, but why do you ignore the empirical elephant in the room? What is your motivation for being so dishonest. This is not a minor point that is going to go away not matter how much you and fellow Darwinists try to obfuscate the matter! You simply have no empirical evidence to give you warrant for your claims that neo-Darwinism can generate the unfathomed levels of integrated complexity being found in life. Moreover, I know that you know that you don’t have the evidence! You are simply too smart to think that you do have the evidence, and yet you continually try to ‘run the distraction’ with your neutral theory gambit, literature bluff, and what not. So wd400 ‘instead of running the distraction’ why donât you, if not for me at least for yourself personally, answer the (following) question honestly? Why do you sacrifice every ounce of your personal integrity and honor, and trash any respect anyone may have had for you as a scientist here on UD, on the pseudo-science that is Darwinian evolution when you can do so much better than that?
Verse:
Gpuccio
Thank you and very well put on why random can never achieve this type of regulatory system. It is being controlled from becoming random in the first place, but you have to ask this… If it did create itself when did it know when to start regulating itself? Can anybody point me to any ordered system that has ever shown that it can built its own regulation and then also regulate itself? Any system at all?
Firstly, what we see here is a real regulation mechanism, I have to ask how does it âknowâ what is to be regulated?
Firstly, what we see here is a real regulation mechanism, I have to ask how does it âknowâ what is to be regulated?
It doesn’t, of course.
The point I was hoping someone would stumble on, is that this paper shows DNA methylation (‘epigenetics’) is itself regulated by plain old genetics. So much for all these posts about the limited power of DNA…
WD400
How does that which is above or over that which is not, get controlled by that which is not above or over it?
Sometimes you can be really funny…..
Epigenetics isn’t “above” genetics, not matter what the bits of the word mean. Afterall, without methyl-transferase genes you wont’ have methylation…
wd400:
The problem is: what tells methyl-transferase which genes should be methylated?
IOWs, protein coding genes produce the effectors (proteins), but where are written the procedures that regulate the expression of different effectors in different cells and situations?
We still don’t understand that. You may believe that everything is written in the genome. That could be true or not, but at present we don’t understand how and where, in the genome or elsewhere, those procedures are coded.
The procedures will be, in the end, much more complex than the effectors. As soon as we understand more of how regulatory procedures are coded, a further severe blow will be struck to the myths of neo darwinism.
The problem is: what tells methyl-transferase which genes should be methylated?
Histones, mainly. And small RNAs and proteins.
You can, of course, keep on regressing deeper, and there is no doubt gene regulation is complex. But we know a lot more about it than you see to think, and this rush to induce outside forces to contol it seems very odd
wd400 you state:
Actually what is odd is that reductive materialists/atheists do not see, or refuse to see, the need for ‘overall context’ in order to make sense of individual things happening in the cell, and in the universe at large.
Dr. John Sanford puts the ‘context problem’ for reductive materialists, and their failure to realize the need for ‘contextual meaning’, like this:
Here is an insightful comment:
Besides the fact that Quantum Mechanics has now falsified reductive materialism as true, it is now known that contextual ‘form’ is a driving force in molecular biology:
etc..etc..
It is simply impossible for a part to arise in isolation to a prior and meaningful whole existing beforehand. The following book review, using Dawkin’s infamous ‘Weasel’, gets that point across very clearly:
Pastor Joe Boot puts the insurmountable ‘context’ problem for reductive materialists this way:
And indeed, given reductive materialism, and its insistence that random unguided forces created everything around us, we have no reason to presuppose that the ‘form’ of the universe to be a circular sphere instead of any number of an infinity of other shapes:
Verse and Music:
wd400:
So much for all these posts about the limited power of DNAâŚ
It’s not that DNA has limited power, it’s that DNA has no power.
It’s like arguing over whether three’s more power in a music CD or in a movie DVD or in a software program that arrives on CD or DVD. They all serve equally well as a coaster. More power to them.
wd400:
I am in no “rush to induce outside forces to contol it”. I just want to make clear what we know and what we don’t know.
You seem to be in a rush to state that we understand what we don’t understand.
It is not simply a problem of regress.
Transcriptomes are many and different and functional and appropriate for different cells and conditions.
The genome is one, always the same in all the cells of one organism (with the two exceptions I mentioned in a previous thread, immune cells and reproductive cells).
Histones, and small RNAs, and proteins, are all made from the same genome, but they are made, or regulated, differently in different cells and in different conditions.
To get different ordered transcriptomes from one single genome, you need intelligent procedures. We don’t know where those procedures are coded, we don’t know how they work.
Let’s make a very simple example. Let’s say, just for the sake of discussion, that as humans we have 20000 protein coding genes (rather accurate), and that we have 1000 different cell types and cell states (just to give a number). Let’s assume for a moment (completely hypothetichal) that each different cell type or cell state translates 10000 genes (probably in different isoforms, nut let’s ignore that further level of complexity for the moment). Let’s ignore also the time sequence in which the genes are translated, and the relative abundance of each gene.
Let’s simplify. We just define each transcriptome, in this thought experiment, by the simple list of the 10000 genes, out of 20000, which are translated in that cell at that moment. So, we have 1000 different lists (one for each cell type or state) of 10000 genes out of 20000 genes in the common genome.
OK. So, how many are the combination of 10000 different genes out of 20000? That is difficult to say, because the statistical program I use (R) cannot give an answer. But I computed the combinations for smaller numbers out of 20000. Here are the results:
> choose(20000,10)
[1] 2.815526e+36
> choose(20000,20)
[1] 4.269216e+67
> choose(20000,30)
[1] 3.960858e+96
> choose(20000,40)
[1] 1.296003e+124
> choose(20000,50)
[1] 3.481789e+150
So, even if only 50 genes have to be sorted out of 20000 as a special combinations, there is a search space of 3.481789e+150. That’s about Dembski’s universal probability bound, if you remember.
For 60 genes, it becomes:
> choose(20000,60)
[1] 1.268095e+176
Well beyond the bound.
Do you understand what I mean when I say that you need definite guiding procedures if you have to select the right genes that have to be translated out of a repertoire of 20000 genes?
And remember, we are overlooking the problem of differential transcription/translation of the same gene, of gene chronological sequence and relative abundance, and many others.
Remember, in the recent paper about the Drosophila transcriptome they showed that 47 genes were translated with more than 1000 isoforms each, in the central nervous system and in the embryo, some of them with up to 800 different proteins translated for the same gene.
So, where are the procedures, and how do they work?
My only purpose here is to outline this important, usually overlooked, question.
You seem satisfied that “we know a lot more about it than I seem to think”.
No. the simple fact is that there is a lot lot more that we don’t know than you seem to think, a lot lot more than what I know we already know.
All I can suggest is that you read a little about gene regulation and development. There’s no way the gene regulation of genes, or the evolution ther of, is a C(n,k) scenario, and it’s not true that the regulation of genes requires intelligence.
As for the Drosophila example, I don’t know but I presume this is one of the ‘deep sequencing’ projects, so it’s likely many of the transcripts are aberrant and in very low number. But, in general, alternative splicing is controlled by regulatory proteins that bind to sites in pre-mRNA to prevent (or hinder) the splicing complex. In most cases, aleternatively spliced mRNAs don’t make radically different proteins (even in extreme cases like Dropshophila’s DScam gene)
You certainly do need methyltransferases…and demethylators (or you cannot switch off from methylated state) and the interpreters of the methylation state. So 3 proteins for the system to work. Chicken or egg?
Funny to bring up histones with their huge number of modifications outside just simple methylation as well, increases complexity to an unimaginable degree. It takes great faith to believe this all happened through evolutionary processes as described by current proponents.
JD
wd400:
You are still evading and equivocating. My simple point is that the regulation of genes requires regulatory procedures, and that those procedures must be written somewhere in some way, if they are transmitted from cell to cell. And we don’t know how and where they are written.
Of course the regulation of genes cannot be a C(n,k) scenario, because otherwise it could not happen. That’s exactly my point. It is not a C(n,k) scenario because it must be controlled by specific procedures, which know exactly what is to be done in different moments, in different cells, and in different circumstances. Call them intelligent or not, as you like. But those procedures must be somewhere.
Again, the genome is the same in all cells of one individual. Transcriptomes are many and different, and they must be chosen accurately out of a nearly infinite search space. Only specific algorithmic procedures can ensure that result. Those procedures must be in the genome or somewhere else in the cell. And we know almost nothing of them. That’s the simple truth.